Cv: Test 2: 13. Maloney: Agents To Treat Hf 2

Front 1

Ms. Heddy Fail’s heart failure is getting worse because she just had an episode of pulmonary edema. Remember before that she had left ventricular hypertrophy and a reduced ejection fraction. What will you use to treat her heart failure?



What stage is she?

Back 1

ACE inhibitor and B Blocker and Diuretic for the edema

Stage C

Front 2

what are the only drugs that will control fluids in people with HF?

Back 2

Diuretics

Front 3

what effect will a loop diuretic have on preload? what does this do to pulmonary edema?

Back 3

decrease it

gets rid of pulmonary edema

Front 4

What effect will diuretics have on CO in a patient with heart failure?

Back 4

Little/no effect

Front 5

Which class of diuretics is most useful in the treatment of edema associated with heart failure?

Back 5

LOOPS

ya know, a jockey, a pro caddy

Front 6

What stage HF do you use loop diuretics?

Back 6

C and D (remember A and B don't have any symptoms!)

Front 7

can thiazide diuretics adequately control fluid retention in HF on their own? what about K sparing?

Back 7

ONLY LOOPS WORK

Front 8

hypokalemia can be an adverse effect of what?

Back 8

Loop diuretics

Front 9

What is one of the major problems associated with K+ or Mg++ depletion?

Back 9

can predispose a patient to cardiac arrhythmias

Front 10

How do you prevent the hypokalemia associated with loop or thiazide diuretics?

Back 10

add a K sparing diuretic

Front 11

_______ levels may be _____ times greater in patients with HF

Back 11

Alsodosterone

20x

Front 12

what two negative effects do high levels of aldosterone have?

Back 12

vascular injury

cardiac remodeling

Front 13

what are the 3 drugs used to prevent remodeling in the heart?

Back 13

ACEi, B blocker, aldosterone antagonists

Front 14

what are the 2 alodosterone antagonists?

Back 14

Spironolactone
Eplerenone

Front 15

What Stage do you use aldosterone antagonists? What NYHA class?

Back 15

Stage C

NYHA Class III-IV

Front 16

A patient has Stage C, NYHA Class III HF. If their serum creatinine is > 2.5 mg/dL (normal 0.8-1.2 mg/dL), would you use an aldosterone antagonist?

why

Back 16

NO

if serum creatinine is high, you want to minimize the risk of life threatening hyperkalemia that would accompany the kidney's lack of filtration

Front 17

A patient has Stage C, NYHA Class III HF. If their serum K is > 5.0 mEq/L (normal 3.5 - 5.0 mEq/L), would you use an aldosterone antagonist?

why

Back 17

NO

you want to minimize the risk of life threatening hyperkalemia

Front 18

What is the advantage in using eprelerenone vs spironolactone ?

Back 18

both are aldosterone antag

eplerenone does not block androgen or progesterone receptors

so it is better

Front 19

Ms. Heddy Fail complains of being pretty fatigued with short walks. She has had to go into the hospital several times for her heart failure. She is on ramipril, metoprolol, eplerenone, and furosemide. What will you use to treat her heart failure?

what stage HF is she?

Back 19

keep her on what she is already, but add in DIGOXIN


Stage C HF.

Front 20

back in the day what was HF known as?

Back 20

Dropsy

Front 21

please list the mech of action for Digoxin, including the different ion exchangers involved

Back 21

inhibits the K/Na ATPase

this increases intracellular Na

This then decreases the activity of the Ca/Na exchanger (meaning less Ca is going out)

Ca is then taken back up via the Ca-ATPase on the SR membrane

thus on the next conduction you can get a huge release of Ca giving you a more forceful contraction (positive inotropic effect)

Front 22

what inhibits digoxin from binding to the extracellular K/Na ATPase?

Back 22

High extracelluar K+

Front 23

What happens if serum K+ is too low or too high with respect to dig use?

Back 23

Hypokalemia will increase the effect/toxicity of digoxin (this is because less potassium will prevent the inhibition of digoxin from binding to the extracellular K/Na ATPase)

Hyperkalemia reduces the action of digoxin

Front 24

What class of drugs can cause hypokalemia? 2

Back 24

Thiazide and loop diuretics

Front 25

Hyperkalemia _____ the action of digoxin

Back 25

reduces

Front 26

what are 2 indirect effects of digoxin? what do these effects lead to?

Back 26

Increases vagal activity

Sensitizes baroreceptors and decreases sympathetic activity

Leads to--> decrease in activity of the SA and AV node

Front 27

at lower doses what is a toxic effect on of digoxin the heart?

Back 27

Sinus bradycardia, AV block
----due to: Excess vagal tone

Front 28

at higher doses what is a toxic effect of digoxin on the heart? 2

Back 28

increased sympathetic tone (centrally induced)

Ca overload

Front 29

What is Ca overload?

Back 29

too much Ca leads to cardiac arrhythmia damage

Front 30

In a damaged heart, what can excessive sympathetic tone and Ca overload cause?

Back 30

cardiac arrhythmias

Front 31

what causes a delayed after depolarization (DAD)? they can be seen with use of?

Back 31

Calcium overload, which leads to a spontaneous release of Ca from the SR, which then leads to the DAD

seen with use of digoxin

Front 32

what is meant by a low therapeutic index? what HF drug has this characteristic?

Back 32

the toxic dose is very close to the therapeutic dose

digoxin

Front 33

Nausea and vomiting can be a side effect of digoxin toxicity...what is dig doing that is causing this?

Back 33

activating the chemoreceptive trigger zone in the brain which leads to nausea and vomiting

Front 34

what is the first sign of digoxin toxicity?

Back 34

they are vomiting, because digoxin is hitting the chemoreceptive trigger zone

Front 35

what does digoxin do in the GI tract?

Back 35

anorexia and diarrhea due to increased motility

Front 36

person is in hospital, on alot of medications but is being treated for heart failure. they start reporting weird dreams and hallucinations...what drug is the culprit?

Back 36

Digoxin

Front 37

a HF patient comes in complaining of green and yellow halos around objects... what is this a side effect of

Back 37

digoxin toxicity

Front 38

gynecomastia can be the result of what 2 drugs

Back 38

spironolactone and digoxin

Front 39

what do you do when you have digoxin toxicity? do you do this if they are nauseous? what if they have a cardiac arrhythmia

Back 39

give FAB fragment of digoxin specific antibody (Digibind)

nauseous: NO, it has too many side effects

arrhythmia: YES, this could kill you

Front 40

Ms. Heddy Fail’s serum creatinine has been increasing (remember she has Stage C HF). Further testing reveals renal artery stenosis. She is on ramipril, metoprolol, digoxin and furosemide. do you want to continue your treatment? anything additional?

Back 40

all except ramipril (renal artery stenosis contraindicates this)

Hydralazine and isosorbide dinitrate

Front 41

mechanism of isosorbide dinitrate? end result?

Back 41

NO to the veins

causes vasodilation

decrease Preload

end result: reduces edema and wall stress

Front 42

mechanism of hydralazine? end result?

Back 42

dilates arteries

decreases afterload

end result: increases ejection fraction and decreases wall stress

Front 43

when do you want to use Isosorbide Dinitrate + Hydralazine?

Back 43

in african american patients

reduces mortality

Front 44

What is the goal in the pharmacological treatment of acute decompensated HF? 2

Back 44

remove pulmonary congestion (edema) if present

decrease pump failure (poor CO), if present

Front 45

How can pulmonary edema be reduced? (2)

Back 45

Loop diuretic (reduced blood volume) or reduce preload

Front 46

how can CO output be increased in acute decompensated HF

Back 46

reduce afterload

increase myocardial contractility

Front 47

when do you want to increase myocardial contractility (what stage)

Back 47

Stage D

Front 48

How can afterload be reduced?

Back 48

arteriodilator

Front 49

please list the 4 IV drugs for acutely decompensated heart failure

Back 49

Loop diuretics
Nitroglycerin
Nitroprusside
Nesiritide

Front 50

What do you have to be concerned about when using loop diuretics for decompensated HF? 4

Back 50

hypotension
worsened renal function
hypokalemia
excessive diuresis

Front 51

What is the best choice for treating congestion or pulmonary edema in a patient with acute decompensated heart failure?

Back 51

Loop diuretic

Front 52

what does nitroglycerin do?

Back 52

increases NO mainly in veins

Front 53

what does nitroprusside do?

Back 53

increase NO in both arteries in veins

Front 54

what is Nesiritide?

Back 54

Recombinant human B-type natriuretic peptide (BNP)

Front 55

what is the MOA of Nesiritiede? (for blood vessels)

Back 55

Activates guanylyl cyclase on vascular smooth muscle cells

this increases cGMP

which vasodilates arteries and veins

Front 56

what is the MOA of Nesiritiede? (for kidney) 3

Back 56

constricts the efferent arteriole and dilates the afferent (leads to increased GFR)

antagonizes Na reabsorption (leads to natiuresis)

Front 57

what is a serious side effect of nesiritide?

Back 57

Worsening of renal function, so don't use with people that have problems with kidneys

also can have possibly increased mortality vs other treatments

Front 58

A 76-year-old male presents in the emergency room with dyspnea. Physical exam reveals 2+ pitting edema, blood pressure of 110/80 and bibasilar rales. He has a history of heart failure (Stage C, NYHA Class II) and hypertension. His current medications include furosemide, ramipril and carvedilol. Which drug would most likely treat his acute problems?

Back 58

IV Furosemide

Front 59

what are the 3 general types of positive inotropic drugs for short term, hemodynamic support in patients with severe heart failure?

Back 59

dobutamine

dopamine

phosphodiesterase inhibitors

Front 60

what is the mechanism of action of dobutamine?

Back 60

activates B1 > B2 > alpha

so it hits the B1 receptor to cause a positive ionotropic effect

and

B2 on vasculature to cause vasodilation

Front 61

does dobutamine cause an increase in HR?

Back 61

NO

even though it activates B1 > B2 > alpha

Front 62

what receptor(s) are affected by dopamine??

Back 62

1st: activates D1
2nd: activates B
3rd: activates alpha

Front 63

how does low dose dopamine work in HF?

Back 63

low dose dopamine hits DA receptors leading to:

Vasodilation of renal, splanchnic, cerebrospinal, and coronary blood vessels

Front 64

how does an intermediate dose of dopamine working in HF?

Back 64

hits B1 receptors

positive inotropic effect

Front 65

how does a high dose of dopamine working in HF? when do you use this?

Back 65

hits a1 receptors

vasoconstriction of arteries

can help if extremely hypotensive with problems profusing organs

Front 66

mechanism of phosphodiesterase inhibitors in acute HF?

Back 66

increase cAMP leading to positive ionotropic effect

Front 67

what is a long term effect of milrinone? what kind of drug is this?

Back 67

this is a PDE III inhibitor....

can cause death with prolonged used

Front 68

what does nitroglycerine do to preload?

what does reduced preload do

Back 68

decreases it

reduces edema

Front 69

how do you reduce edema?

Back 69

reduce preload...aka vasodilate veins

Front 70

for a patient in severe HF (stage D) what are the 3 drugs you want to be thinking about giving?

Back 70

Dobutamine

Dopamine

PDE Inhibitors (Milrinone)

Front 71

For stage A HF, what drugs should your pt be on?

Back 71

ACE inhibitor/ARB

Front 72

For stage B HF, what drugs should your pt be on?

Back 72

ACE inhibitor/ARB + B Blocker

Front 73

For stage C HF, what drugs should your pt be on?

Back 73

ACE inhibitor/ARB
B Blocker
Diuretic
Digoxin
Aldosterone antag

Front 74

For stage D HF, what drugs should your pt be on?

Back 74

ACE inhibitor/ARB
B Blocker
Diuretic
Digoxin
Aldosterone antag
and positive ionotropic effect drug (IV)